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Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
Published on: August 3, 2018
miR-92a-3p promotes pulmonary fibrosis progression by regulating KLF2-mediated endothelial-to-mesenchymal transition
1Division of Geriatric Cardiology, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029 People's Republic of China.
Abstract:
Pulmonary fibrosis (PF) is a chronic lung disease that has a poor prognosis and a serious impact on the quality of life of patients. Here, we investigated the potential role of miR-92a-3p in PF. The mRNA level of miR-92a-3p was significantly increased in both the lung tissues of bleomycin (BLM)--treated mice and pulmonary microvascular endothelial cells (PMVECs). Overexpressing miR-92a-3p increased the mRNA and protein levels of α‑SMA, vimentin, and Col-1 but downregulated E-cadherin. Additionally, the protein and mRNA expression levels of KLF2 were significantly decreased in the lung tissues of BLM-treated mice, suggesting that KLF2 participated in the progression of BLM-induced PF. Downregulating miR-92a-3p upregulated the expression of KLF2 and inhibited the endothelial-to-mesenchymal transition (EndoMT) process, thus alleviating PF in vivo. Altogether, a miR-92a-3p deficiency could significantly reduce the development of myofibroblasts and ameliorate PF progression.
Insights
MicroRNA-92a-3p (miR-92a-3p) promotes pulmonary fibrosis (PF) by driving endothelial-to-mesenchymal transition. Inhibiting miR-92a-3p alleviates PF progression and myofibroblast development in mice.
Area of Science:
- Biomedical Research
- Molecular Biology
- Pulmonary Medicine
Background:
- Pulmonary fibrosis (PF) is a severe chronic lung disease with limited treatment options.
- The molecular mechanisms underlying PF progression, particularly the role of microRNAs, require further elucidation.
Purpose of the Study:
- To investigate the role of microRNA-92a-3p (miR-92a-3p) in the pathogenesis of pulmonary fibrosis.
- To explore the potential of targeting miR-92a-3p as a therapeutic strategy for PF.
Main Methods:
- Assessed miR-92a-3p expression in bleomycin (BLM)-induced mouse lung tissues and pulmonary microvascular endothelial cells (PMVECs).
- Manipulated miR-92a-3p levels to observe effects on fibrosis markers (α‑SMA, vimentin, Col-1, E-cadherin) and KLF2 expression.
- Evaluated the impact of miR-92a-3p downregulation on endothelial-to-mesenchymal transition (EndoMT) and PF progression in vivo.
Main Results:
- miR-92a-3p expression was significantly upregulated in BLM-induced PF models.
- Overexpression of miR-92a-3p promoted fibrosis markers and downregulated E-cadherin, while decreasing KLF2 expression.
- Downregulation of miR-92a-3p reversed these effects, inhibited EndoMT, and ameliorated PF in vivo.
Conclusions:
- miR-92a-3p plays a critical role in promoting pulmonary fibrosis by facilitating EndoMT.
- KLF2 is involved in the progression of BLM-induced PF and its expression is negatively regulated by miR-92a-3p.
- Targeting miR-92a-3p deficiency offers a promising therapeutic approach to reduce myofibroblast development and alleviate pulmonary fibrosis.
